Temperature Regulation during Cold Water Immersion is Modified by Normobaric Hypoxia

Abstract

Purpose Indigenous diving populations and recreational breath-hold divers often develop hypoxia while diving in cold water. Hypoxia may delay the onset and reduce magnitude of shivering during cold exposure. It is unclear if these hypoxia-induced alterations in the control of shivering reduce total energy expenditure, a function of both shivering and non-shivering thermogenesis, and/or modify the ability to maintain core temperature during cold water immersion. Therefore, this study tested the hypothesis that normobaric hypoxia decreases total energy expenditure and results in a greater decrease in core temperature during one hour of head out cold water immersion. Methods In a randomized crossover design, 6 healthy adults (27 ± 2 y, 1 woman) completed one hour of head out cold (22°C) water immersion breathing either normobaric normoxia (FiO2 = 0.21) or normobaric hypoxia (FiO2 = 0.13). Data were collected for 10 minutes prior to water immersion (baseline) and during water immersion. Energy expenditure was estimated from oxygen consumption (V̇O2) and respiratory exchange ratio (RER) measured via indirect calorimetry. Arterial oxyhemoglobin saturation (SpO2) was estimated using pulse oximetry on the forehead. Rectal temperature was used to estimate core temperature. Brown adipose tissue activation was estimated by measuring bilateral supraclavicular skin temperature. In a subset of subjects (n = 2) skin temperature was measured bilaterally on the back over the trapezius muscle, to confirm the unique profile of changes in supraclavicular skin temperature. Data during cold water immersion were compared relative to the last two-minutes of baseline and integrated throughout water immersion (60 minutes). Data are presented as mean ± SD. Results During water immersion, SpO2 was lower in hypoxia (90 ± 3%) compared to normoxia (98 ± 2%, P < 0.01). Baseline rectal temperature was not different between hypoxia (37.3 ± 0.2°C) and normoxia (37.4 ± 0.2°C, P = 0.52). At the end of water immersion, rectal temperature in hypoxia (36.6 ± 0.4°C) was lower than in normoxia (36.9 ± 0.3°C, P < 0.01). No differences in the total increase above baseline during water immersion were observed in V̇O2 (Hypoxia: 28.3 ± 7.2L; Normoxia: 29.5 ± 6.8 L, P = 0.74) or energy expenditure (Hypoxia: 191 ± 69 KJ·min; Normoxia: 143 ± 81 KJ·min, P = 0.32) between trials. Supraclavicular skin temperature increased with water immersion (P < 0.01), while back skin temperature decreased (P = 0.02). No differences were observed in the total increase from baseline in supraclavicular skin temperature (Hypoxia: 66.6 ± 30.3°C·min; Normoxia: 66.1 ± 35.3°C·min, P = 0.54) or total decrease from baseline in back skin temperature (Hypoxia: -42.3 ± 30.8°C·min; Normoxia: -56.6 ± 7.9 °C·min, P = 0.14). Conclusions These preliminary findings support that, compared to normoxia, normobaric hypoxia promotes a greater reduction in core temperature during one hour of head out cold water immersion. The mechanism(s) underlying this observation remains unclear as no differences in energy expenditure and brown adipose tissue activation were observed, but alterations in cutaneous blood flow cannot be excluded.